Diabetologia

, Volume 30, Issue 5, pp 333–343

Aberrant expression of Class II major histocompatibility complex molecules by B cells and hyperexpression of Class I major histocompatibility complex molecules by insulin containing islets in Type 1 (insulin-dependent) diabetes mellitus

Authors

  • A. K. Foulis
    • University Department of PathologyRoyal Infirmary
  • M. A. Farquharson
    • University Department of PathologyRoyal Infirmary
  • R. Hardman
    • University Department of PathologyRoyal Infirmary
Originals

DOI: 10.1007/BF00299027

Cite this article as:
Foulis, A.K., Farquharson, M.A. & Hardman, R. Diabetologia (1987) 30: 333. doi:10.1007/BF00299027

Summary

Twenty-three patients with recent onset Type 1 (insulin-dependent) diabetes in whom residual insulin secreting B cells were present and 12 patients with disease of more prolonged duration (maximum 9 years), 8 of whom had residual B cells, were studied. Aberrant expression of Class II major histocompatibility complex molecules was demonstrated immunohistochemically on insulin secreting B cells in 21 out of 23 patients with recent onset disease and 6 of the patients with more prolonged disease. No such expression was seen on glucagon secreting A cells or somatostatin secreting D cells. Islets where there was marked hyperexpression of Class I major histocompatibility complex molecules on islet endocrine cells were seen in all cases in which residual B cells were present. Ninety-two per cent of insulin containing islets but only 1% of insulin deficient islets exhibited this phenomenon (p<0.001, Chi-squared test). There was evidence to suggest that both these abnormalities of major histocompatibility complex expression preceded insulitis within a given islet. They also appeared to be unique to Type 1 diabetes, being absent in pancreases of patients with Type 2 (non-insulin-dependent) diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to B cells in Type 1 diabetes may be a “multistep” process in which abnormalities of major histocompatibility complex expression on islet endocrine cells are crucial events.

Key words

Pancreasislets of Langerhansantigen-immune responseautoimmunityType 1 diabetes mellitusmajor histocompatibility complex

Copyright information

© Springer-Verlag 1987